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Featured researches published by M Campone.


British Journal of Cancer | 2014

Randomised proof-of-concept phase II trial comparing targeted therapy based on tumour molecular profiling vs conventional therapy in patients with refractory cancer: results of the feasibility part of the SHIVA trial

C. Le Tourneau; Xavier Paoletti; Nicolas Servant; I. Bieche; David Gentien; T. Rio Frio; Anne Vincent-Salomon; Vincent Servois; Julien Roméjon; Odette Mariani; Virginie Bernard; P Huppe; Gaëlle Pierron; F. Mulot; Céline Callens; J Wong; Cecile Mauborgne; Etienne Rouleau; C Reyes; E Henry; Quentin Leroy; Pierre Gestraud; P La Rosa; L Escalup; Emmanuel Mitry; Olivier Tredan; J-P Delord; M Campone; Anthony Gonçalves; N. Isambert

Background:The SHIVA trial is a multicentric randomised proof-of-concept phase II trial comparing molecularly targeted therapy based on tumour molecular profiling vs conventional therapy in patients with any type of refractory cancer. Results of the feasibility study on the first 100 enrolled patients are presented.Methods:Adult patients with any type of metastatic cancer who failed standard therapy were eligible for the study. The molecular profile was performed on a mandatory biopsy, and included mutations and gene copy number alteration analyses using high-throughput technologies, as well as the determination of oestrogen, progesterone, and androgen receptors by immunohistochemistry (IHC).Results:Biopsy was safely performed in 95 of the first 100 included patients. Median time between the biopsy and the therapeutic decision taken during a weekly molecular biology board was 26 days. Mutations, gene copy number alterations, and IHC analyses were successful in 63 (66%), 65 (68%), and 87 (92%) patients, respectively. A druggable molecular abnormality was present in 38 patients (40%).Conclusions:The establishment of a comprehensive tumour molecular profile was safe, feasible, and compatible with clinical practice in refractory cancer patients.


Cancer Research | 2011

S3-7: Everolimus for Postmenopausal Women with Advanced Breast Cancer: Updated Results of the BOLERO-2 Phase III Trial.

Gabriel N. Hortobagyi; Martine Piccart; H Rugo; Howard A. Burris; M Campone; Shinzaburo Noguchi; Michael Gnant; Kathleen I. Pritchard; Luc Vittori; P Mukhopadhyay; Tarek Sahmoud; David Lebwohl; José Baselga

Background: The mTOR pathway is constitutively activated in hormone-resistant advanced breast cancer (ABC). In phase II trials, everolimus (EVE) showed promising efficacy both as monotherapy and in combination with endocrine therapy in patients with estrogen receptor-positive (ER+) ABC. This double-blind, placebo-controlled, phase III study evaluated EVE plus exemestane (EXE) in patients with ER+ ABC refractory to letrozole or anastrozole. Patients and Methods: Eligible patients were randomized (2:1) to EXE (25 mg/day) with EVE (10 mg/day) or with matching placebo. The primary endpoint was progression-free survival (PFS). Secondary endpoints included overall survival, response rate, quality of life (QoL), and safety. Results: 724 patients were randomized (485: EVE+EXE; 239: EXE). Baseline characteristics were well balanced; median age was 62 years, 56% had visceral involvement, and 84% had documented benefit from previous endocrine therapy, which included letrozole or anastrozole (100%), tamoxifen (48%), fulvestrant (16%), and chemotherapy for advanced disease (25%). This analysis is based on 457 events and median follow-up of 12.5 months. PFS by investigator assessment showed a hazard ratio (HR) of 0.44 (95% CI: 0.36−0.53) and a median duration of 7.4 (EVE+EXE) vs 3.2 months (EXE) (P The most common grade 3/4 adverse events were stomatitis (8% vs 1%), anemia (7% vs 1%), hyperglycemia (5% vs Conclusion: The addition of EVE to EXE is associated with significant and sustained prolongation of PFS. Adverse events were higher in the combination arm but manageable by dose interruption and/or reduction and did not affect QoL. EVE in combination with an aromatase inhibitor is a promising therapeutic option for women with hormone receptor-positive advanced breast cancer. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr S3-7.


Cancer Research | 2016

Abstract S6-01: PIK3CA status in circulating tumor DNA (ctDNA) predicts efficacy of buparlisib (BUP) plus fulvestrant (FULV) in postmenopausal women with endocrine-resistant HR+/HER2– advanced breast cancer (BC): First results from the randomized, phase III BELLE-2 trial

J. Baselga; S-A Im; Hiroji Iwata; Mark Clemons; Yoshinori Ito; Ahmad Awada; Stephen Chia; Agnieszka Jagiełło-Gruszfeld; Barbara Pistilli; L-M Tseng; S. Hurvitz; Norikazu Masuda; Javier Cortés; M. De Laurentiis; Carlos L. Arteaga; Z Jiang; Walter Jonat; Soulef Hachemi; S Le Mouhaër; E Di Tomaso; Patrick Urban; Cristian Massacesi; M Campone

Background: PI3K pathway activation is a hallmark of hormone receptor-positive (HR+) BC cells resistant to endocrine therapy (ET). Preclinical and early clinical data suggest that combining the pan-PI3K inhibitor BUP (BKM120) with ET may provide clinical benefits in this setting. BELLE-2 (NCT01610284) is the first randomized Phase III trial to assess the efficacy and safety of a PI3K inhibitor combined with FULV in HR+ advanced BC, including a prospective analysis of whether PI3K pathway activation status measured in archival tumor tissue and ctDNA is predictive of clinical benefit. Methods: Postmenopausal women with HR+/HER2– locally advanced or metastatic BC refractory to aromatase inhibitor therapy were enrolled. After a 14-day run-in with FULV (500 mg), patients (pts) were randomized (1:1) to receive oral BUP (100 mg/day) or placebo (PBO) with FULV (500 mg per standard of care). Randomization of all pts was stratified by PI3K pathway status measured in archival tumor tissue (PIK3CA mutation or PTEN loss; activated, non-activated, unknown) and visceral disease status (present, absent). Baseline PIK3CA mutation status in ctDNA was assessed in a subset of 587 pts at trial entry. The primary endpoint was locally-assessed progression-free survival (PFS; RECIST v1.1) in the full population and PI3K pathway-activated group. Secondary endpoints included overall survival, safety, overall response rate (ORR), and clinical benefit rate (CBR). Results: 1147 pts received FULV with BUP or PBO, with 187 (16%) ongoing at data cut-off. Baseline characteristics were well balanced between the two arms: median age was 62 years, 98% had ECOG performance status of 0/1, 61% had visceral disease, 69% were sensitive to prior ET, 28% had received prior chemotherapy for metastatic BC. BELLE-2 met its primary endpoint in the full population (Table). In pts with PI3K pathway-activated tumor tissue, PFS increase for BUP+FULV vs PBO+FULV did not meet the planned endpoint. Among pts with PIK3CA status measured in ctDNA, median PFS, ORR, and CBR were significantly improved for BUP+FULV vs PBO+FULV in pts with PIK3CA-mutant tumors but not pts without. The most common Grade 3/4 adverse events (AEs; ≥5% of pts; BUP+FULV vs PBO+FULV) in all pts were increased alanine aminotransferase (26 vs 1%), increased aspartate aminotransferase (18 vs 3%), hyperglycemia (15 vs 0.2%), and rash (8 vs 0%). The most common reasons for treatment discontinuation were disease progression (54 vs 73%) and AEs (13 vs 2%). Conclusions: BELLE-2 met its primary endpoint in the full population. Prespecified analyses showed that characterizing PIK3CA mutation in ctDNA at trial entry identifies pts with endocrine- resistant HR+/HER2–advanced BC, for whom BUP+FULV results in meaningful clinical benefits. Citation Format: Baselga J, Im S-A, Iwata H, Clemons M, Ito Y, Awada A, Chia S, Jagiello-Gruszfeld A, Pistilli B, Tseng L-M, Hurvitz S, Masuda N, Cortes J, De Laurentiis M, Arteaga CL, Jiang Z, Jonat W, Hachemi S, Le Mouhaer S, Di Tomaso E, Urban P, Massacesi C, Campone M. PIK3CA status in circulating tumor DNA (ctDNA) predicts efficacy of buparlisib (BUP) plus fulvestrant (FULV) in postmenopausal women with endocrine-resistant HR+/HER2– advanced breast cancer (BC): First results from the randomized, phase III BELLE-2 trial. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr S6-01.


Annals of Oncology | 2015

Randomized, phase II, placebo-controlled trial of onartuzumab and/or bevacizumab in combination with weekly paclitaxel in patients with metastatic triple-negative breast cancer

V. Dieras; M Campone; Denise A. Yardley; Gilles Romieu; V. Valero; Steven J. Isakoff; H. Koeppen; Timothy R. Wilson; Y. Xiao; D. S. Shames; S. Mocci; M. Chen; P. Schmid

BACKGROUNDnIncreased hepatocyte growth factor/MET signaling is associated with an aggressive phenotype and poor prognosis in triple-negative breast cancer (TNBC). We evaluated the benefit of adding onartuzumab, a monoclonal anti-MET antibody, to paclitaxel with/without bevacizumab in patients with TNBC.nnnPATIENTS AND METHODSnWomen with metastatic TNBC were randomized to receive onartuzumab plus placebo plus weekly paclitaxel (OP; n = 60) or onartuzumab plus bevacizumab plus paclitaxel (OBP; n = 63) or placebo plus bevacizumab plus paclitaxel (BP; n = 62). The primary end point was progression-free survival (PFS); additional end points included overall survival (OS), objective response rate (ORR), and safety. This trial was hypothesis generating and did not have power to detect minimum clinically meaningful differences between treatment arms.nnnRESULTSnThere was no improvement in PFS with the addition of onartuzumab to BP [hazard ratio (HR), 1.08; 95% confidence interval (CI) 0.69-1.70]; the risk of a PFS event was higher with OP than with BP (HR, 1.74; 95% CI 1.13-2.68). Most patients had MET-negative tumors (88%); PAM50 subtype analysis showed basal-like tumors in 68% of samples. ORR was higher in the bevacizumab arms (OBP: 42.2%; 95% CI 28.6-57.1; BP: 54.7%; 95% CI 41.0-68.4) compared with OP (27.5%; 95% CI 15.9-40.6). Median OS was shorter with OBP (HR, 1.36; 95% CI 0.75-2.46) and OP (HR, 1.92; 95% CI 1.03-3.59), than with BP. Peripheral edema was more frequent in the onartuzumab arms (OBP, 51.8%; OP, 58.6%) versus BP (17.7%).nnnCONCLUSIONnThis study did not show a clinical benefit of the addition of onartuzumab to paclitaxel with/without bevacizumab in patients with predominantly MET-negative TNBC.nnnCLINICALTRIALSGOVnNCT01186991.


Annals of Oncology | 2013

Circulating tumor cells and brain metastasis outcome in patients with HER2-positive breast cancer: the LANDSCAPE trial

Jean-Yves Pierga; François-Clément Bidard; Claire Cropet; P. Tresca; F. Dalenc; Gilles Romieu; M Campone; C. Mahier Aït-Oukhatar; E. Le Rhun; A Goncalves; Marianne Leheurteur; Julien Domont; Maya Gutierrez; Hervé Curé; J-M Ferrero; C. Labbe-Devilliers; Thomas Bachelot

BACKGROUNDnDecrease of circulating tumor cells (CTC) during treatment is an independent prognostic factor in metastatic breast cancer (MBC). We specifically evaluated the impact of CTC on brain metastasis outcome.nnnMETHODSnHER2-positive MBC with brain metastasis not previously treated with whole-brain radiotherapy received first-line combination of lapatinib and capecitabine in a phase II study. CTC were detected at baseline and day 21 (CellSearch).nnnRESULTSnMedian follow-up of the 44 analyzed patients was 21.2 months. The central nervous system objective response (CNS-OR) rate was 66%. At baseline, 20 of 41 assessable patients for CTC (49%) had ≥1 CTC (range 1-301, median 3) and 9 (22%) had ≥5 CTC. At day 21, 7 of 38 patients (18%) had ≥1 CTC (P = 0.006, versus baseline), and CTC had disappeared in 11 patients. CNS-OR rate was significantly higher in patients with no CTC at day 21 [25 of 31 (80%) versus 2 of 7 (29%), P = 0.01]. The 1-year overall survival rate was 83.9% in patients with no CTC at day 21 versus 42.9% in patients with ≥1 CTC (P = 0.02).nnnCONCLUSIONSnThis is the first report showing a correlation between CNS metastasis response, outcome and early CTC clearance under targeted treatment of HER2+ MBC.nnnCLINICAL TRIALS NUMBERnNCT00967031.


Annals of Oncology | 2014

REBECA: a phase I study of bevacizumab and whole-brain radiation therapy for the treatment of brain metastasis from solid tumours

Christelle Levy; D. Allouache; J. Lacroix; A. E. Dugué; S. Supiot; M Campone; M. Mahe; S. Kichou; Marianne Leheurteur; C. Hanzen; V. Dieras; Youlia M. Kirova; F. Campana; E. Le Rhun; L. Gras; Thomas Bachelot; Marie-Pierre Sunyach; I. Hrab; J. Geffrelot; Katharina Gunzer; J.-M. Constans; J.-M. Grellard; B. Clarisse; Xavier Paoletti

C. Lévy1, D. Allouache1, J. Lacroix2,3, A. E. Dugué4, S. Supiot5, M. Campone5, M. Mahe6, S. Kichou2, M. Leheurteur7, C. Hanzen8, V. Dieras9, Y. Kirova10, F. Campana10, E. Le Rhun11, L. Gras12, T. Bachelot13, M.-P. Sunyach14, I. Hrab1, J. Geffrelot15, K. Gunzer1,4, J.-M. Constans3,16, J.-M. Grellard4, B. Clarisse4 & X. Paoletti17 Departments of Oncology; Radiology, Centre François Baclesse, Caen; GIP Cyceron, Caen; Department of Clinical Research, Centre François Baclesse, Caen; Departments of Oncology; Radiotherapy, Institut de Cancérologie de l’Ouest René Gauducheau, Nantes-Saint Herblain, Caen; Departments of Oncology; Radiotherapy, Centre Henri Becquerel, Rouen; Departments of Oncology; Radiotherapy, Institut Curie, Paris; Departments of Oncology; Radiotherapy, Centre Oscar Lambret, Lille; Departments of Oncology; Radiotherapy, Centre Léon Bérard, Lyon; Department of Radiotherapy, Centre François Baclesse, Caen; Department of Radiology, Centre Hospitalier Universitaire, Caen; Department of Biostatistics, Institut Curie/Inserm U900, Paris, France


Annals of Oncology | 2016

A randomized adaptive phase II/III study of buparlisib, a pan-class I PI3K inhibitor, combined with paclitaxel for the treatment of HER2- advanced breast cancer (BELLE-4).

Miguel Martin; Arlene Chan; Luc Dirix; Joyce O’Shaughnessy; Roberto Hegg; Alexey Manikhas; Mikhail Shtivelband; P. Krivorotko; N. Batista López; M Campone; M. Ruiz Borrego; Qamar J. Khan; Jt Beck; M. Ramos Vázquez; Patrick Urban; S. Goteti; E. Di Tomaso; Cristian Massacesi; Suzette Delaloge

BackgroundnPhosphatidylinositol 3-kinase (PI3K) pathway activation in preclinical models of breast cancer is associated with tumor growth and resistance to anticancer therapies, including paclitaxel. Effects of the pan-Class I PI3K inhibitor buparlisib (BKM120) appear synergistic with paclitaxel in preclinical and clinical models.nnnPatients and methodsnBELLE-4 was a 1:1 randomized, double-blind, placebo-controlled, adaptive phase II/III study investigating the combination of buparlisib or placebo with paclitaxel in women with human epidermal growth factor receptor 2-negative locally advanced or metastatic breast cancer with no prior chemotherapy for advanced disease. Patients were stratified by PI3K pathway activation and hormone receptor status. The primary endpoint was progression-free survival (PFS) in the full and PI3K pathway-activated populations. An adaptive interim analysis was planned following the phase II part of the study, afteru2009≥125 PFS events had occurred in the full population, to decide whether the study would enter phase III (in the full or PI3K pathway-activated population) or be stopped for futility.nnnResultsnAs of August 2014, 416 patients were randomized to receive buparlisib (207) or placebo (209) with paclitaxel. At adaptive interim analysis, there was no improvement in PFS with buparlisib versus placebo in the full (median PFS 8.0 versus 9.2 months, hazard ratio [HR] 1.18), or PI3K pathway-activated population (median PFS 9.1 versus 9.2 months, HR 1.17). The study met protocol-specified criteria for futility in both populations, and phase III was not initiated. Median duration of study treatment exposure was 3.5 months in the buparlisib arm versus 4.6 months in the placebo arm. The most frequent adverse events with buparlisib plus paclitaxel (≥40% of patients) were diarrhea, alopecia, rash, nausea, and hyperglycemia.nnnConclusionsnAddition of buparlisib to paclitaxel did not improve PFS in the full or PI3K pathway-activated study population. Consequently, the trial was stopped for futility at the end of phase II.


Annals of Oncology | 2016

Paclitaxel plus bevacizumab or paclitaxel as first-line treatment for HER2-negative metastatic breast cancer in a multicenter national observational study.

Suzette Delaloge; David Pérol; C. Courtinard; Etienne Brain; Bernard Asselain; Thomas Bachelot; M. Debled; V. Dieras; M Campone; Christelle Levy; William Jacot; V. Lorgis; Corinne Veyret; F. Dalenc; J-M Ferrero; L. Uwer; Pierre Kerbrat; Anthony Gonçalves; Marie-Ange Mouret-Reynier; Thierry Petit; C. Jouannaud; Laurence Vanlemmens; G. Chenuc; T. Guesmia; M. Robain; C. Cailliot

BACKGROUNDnBevacizumab combined with paclitaxel as first-line chemotherapy for patients with HER2-negative metastatic breast cancer (MBC) has led to mixed results in randomized trials, with an improvement in progression-free survival (PFS) but no statistically significant overall survival (OS) benefit. Real-life data could help in assessing the value of this combination.nnnPATIENTS AND METHODSnThis study aimed to describe the outcome following first-line paclitaxel with or without bevacizumab in the French Epidemiological Strategy and Medical Economics (ESME) database of MBC patients, established in 2014 by Unicancer. The primary and secondary end points were OS and PFS, respectively.nnnRESULTSnFrom 2008 to 2013, 14 014 MBC patient files were identified, including 10 605 patients with a HER2-negative status. Of these, 3426 received paclitaxel and bevacizumab (2127) or paclitaxel (1299) as first-line chemotherapy. OS adjusted for major prognostic factors was significantly longer in the paclitaxel and bevacizumab group compared with paclitaxel [hazard ratio (HR) 0.672, 95% confidence interval (CI) 0.601-0.752; median survival time 27.7 versus 19.8 months]. Results were consistent in all supportive analyses (using a propensity score for adjustment and as a matching factor for nested case-control analyses) and sensitivity analyses. Similar results were observed for the adjusted PFS, favoring the combination (HR 0.739, 95% CI 0.672-0.813; 8.1 versus 6.4 months).nnnCONCLUSIONSnIn this large-scale, real-life setting, patients with HER2-negative MBC who received paclitaxel plus bevacizumab as first-line chemotherapy had a significantly better OS and PFS than those receiving paclitaxel. Despite robust methodology, real-life data are exposed to important potential biases, and therefore, results need to be treated with caution. Our data cannot therefore support extension of current use of bevacizumab in MBC.


Annals of Oncology | 2016

Randomized phase II trial comparing molecularly targeted therapy based on tumor molecular profiling versus conventional therapy in patients with refractory cancer: cross-over analysis from the SHIVA trial

L. Belin; Maud Kamal; Cecile Mauborgne; Corine Plancher; F. Mulot; Jean-P. Delord; A Goncalves; Celine Gavoille; Coraline Dubot; N. Isambert; M Campone; O. Trédan; Francesco Ricci; Marie Alt; Delphine Loirat; M.P. Sablin; Xavier Paoletti; Vincent Servois; C. Le Tourneau

BackgroundnSeveral studies used the ratio of progression-free survival (PFS) on genotype-matched treatment to PFS on genotype-unmatched treatment to assess the efficacy of therapy guided by patients tumor molecular profiling. We evaluated the PFS ratio from patients who cross-over in the SHIVA trial.nnnPatients and methodsnThe primary end point of the SHIVA trial was to compare PFS on molecularly targeted agents (MTAs) based on tumor molecular profiling and treatment at physicians choice (TPC) in patients with any kind of cancer who had failed standard-of-care therapy. The experimental treatment included only marketed MTAs given outside their indications according to a pre-specified treatment algorithm. Patients were allowed to cross-over at disease progression in both arms. Response was evaluated according to RECIST 1.1 at randomization and at cross-over. We evaluated the ratio of PFS on MTA (PFSMTA) to PFS on TPC (PFSTPC) in patients who crossed-over.nnnResultsnAmong 741 patients enrolled in the SHIVA trial, 197 were randomized, and 95 crossed-over, including 70 patients from the TPC to the MTA arm and 25 patients from the MTA to the TPC arm. Two patients crossed-over in the TPC arm without disease progression. The PFSMTA/PFSTPC ratio exceeded 1.3 in 37% of patients who crossed-over from the TPC to the MTA arm. The PFSMTA/PFSTPC ratio exceeded 1.3 in 61% of patients who crossed-over from the MTA arm to the TPC arm.nnnConclusionsnThe cross-over analysis of the SHIVA trial identified 37% of patients who crossed-over from TPC to MTA with a PFSMTA/PFSTPC ratio exceeding 1.3.


Annals of Oncology | 2014

351OGENOMIC AND IMMUNE CHARACTERIZATION OF METASTATIC BREAST CANCER (MBC): AND ANCILLARY STUDY OF THE SAFIR01 & MOSCATO TRIALS

Monica Arnedos; Thomas Filleron; Maria Vittoria Dieci; J. Adam; Paul B. Robbins; Sherene Loi; M Campone; Hervé Bonnefoi; V. Dieras; F. Dalenc; Marta Jimenez; Celine Lefebvre; F. Andre; Thomas Bachelot; Magali Lacroix-Triki

ABSTRACT Aim: So far, little is known about immune and genomic landscape in metastatic breast cancer (mBC). Methods: Patients were retrospectively identified from SAFIR01 and MOSCATO studies that performed molecular screening from a biopsy of a metastatic lesion. Whole exome sequencing (WES) was performed using Hi-Seq technology. Coverage was 50x and 100x for normal and tumoral tissue respectively. Bioinformatic analyses reported mutations and copy number alterations. Immune characterisation was determined by the presence of intratumoral and stromal TILs with PD1 and PDL1 expression assessed by IHC (internal protocol, Medimmune). We correlated tumor characteristics and immune and genomics data. Results: 280 samples were stained for immune analyses. Using a 50% cut-off, few tumors presented intratumoral (n = 3/244, 1%) and stromal (n = 11/244, 5%) TILs. This rate was significantly higher in HER2+ tumors (stromal TIL, 16%; p = 0.0002). Positivity for PD1 (n = 14/252, 5%) and PDL1 (n = 7/255, 3%) were rare, compared to reported in other tumor types. A trend towards higher PDL1 was observed in HER2+ mBC (8.3%; p = 0.0653). Ninety-three samples were analysed for WES with 17 genes found mutated in >3 samples (p Conclusions: This is the first study that assesses both immune and genomic landscapes in mBC. We observed that mBC dramatically differs from primary tumors, and is enriched in genes potentially involved in resistance mechanisms (ESR1, TSC1) or migration process (FRAS1, SCAPER). TILs, PD1, PDL1 are at very low frequency in metastatic lesions, except for Her2 + ++ mBC. Our results suggest that other immune suppressor networks are involved in mBC. Therefore, CD73, CD39 and FoxP3 are being analysed and will be presented. Disclosure: P.B. Robbins: Salary from Medimmune, Inc. All other authors have declared no conflicts of interest.

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A Goncalves

Aix-Marseille University

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Thierry Petit

University of Strasbourg

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